IL1B and brain disorder: This then leads to the activation of pro-inflammatory cytokines interleukin (IL)-1β, IL-18, and IL-33 (Arend et al., 2008; Chakraborty et al., 2010), which promote a number of innate immune processes associated with infection, inflammation and autoimmunity (Davis et al., 2011), thereby responsible for neuroinflammation and associated brain diseases (Tha et al., 2000; Cacquevel et al., 2004; Felderhoff-Mueser et al., 2005; Godbout and Johnson, 2009; Mawhinney et al., 2011; Zhang et al., 2014).